Abstract
Upon touch, twitch once zebrafish respond with one or two swimming strokes instead of typical full-blown escapes. This use-dependent fatigue is shown to be a consequence of a mutation in the tetratricopeptide domain of muscle rapsyn, inhibiting formation of subsynaptic acetylcholine receptor clusters. Physiological analysis indicates that reduced synaptic strength, attributable to loss of receptors, is augmented by a potent postsynaptic depression not seen at normal neuromuscular junctions. The synergism between these two physiological processes is causal to the use-dependent muscle fatigue. These findings offer insights into the physiological basis of human myasthenic syndrome and reveal the first demonstration of a role for rapsyn in regulating synaptic function.
Original language | English (US) |
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Pages (from-to) | 6491-6498 |
Number of pages | 8 |
Journal | Journal of Neuroscience |
Volume | 22 |
Issue number | 15 |
DOIs | |
State | Published - Aug 1 2002 |
Externally published | Yes |
Keywords
- Muscle fatigue
- Myasthenia gravis
- Rapsyn
- Synapse development
- Synaptic depression
- Tetratricopeptide repeats
ASJC Scopus subject areas
- General Neuroscience